Print Quick Response Code in Objective-C Lyme Disease

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Lyme disease, caused by the spirochete Borrelia burgdorferi and transmitted by ticks of the Ixodes genus, may have protean manifestation, but over 75% of patients have symptoms involving the head and neck Facial paralysis, dysesthesias, dysgeusia, or other cranial neuropathies are most common Headache, pain, and cervical lymphadenopathy may occur See 34 for a more detailed discussion

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About 10% of lymphomas present in the head and neck Lymphoma arising in AIDS patients is an increasing concern Multiple rubbery nodes, especially in the young adult, are suggestive of this disease A thorough physical examination may demonstrate other sites of nodal or organ involvement FNA biopsy may be diagnostic, but open biopsy is often required to determine architecture and an appropriate treatment course

Dyspnea is a common symptom It is analogous to hunger or nausea in that sensory input from multiple sites is integrated in the cerebral cortex In general, dyspnea increases with the level of functional impairment as measured by spirometry However, there is only a weak correlation between the severity of dyspnea and quantitative measures of airflow limitation or exercise tolerance Several pathophysiologic processes contribute to dyspnea The most important is the increased respiratory effort that accompanies many different diseases: airflow obstruction (asthma; chronic obstructive pulmonary disease [COPD]), changes in pulmonary compliance (interstitial fibrosis, congestive heart failure) or chest wall compliance (obesity, pleural disease), intrinsic respiratory muscle weakness (inanition, neuromuscular disease, chronic respiratory failure), or the weakness conveyed by the mechanical disadvantage of hyperinflation (asthma or emphysema) Dyspnea is magnified by increased respiratory drive Acute hypercapnia is therefore a potent stimulus to dyspnea, while hypoxemia is usually a weak one Stimulation of irritant receptors in the airways intensifies dyspnea, while stimulation of pulmonary stretch receptors decreases it In mechanically ventilated patients, failure to provide adequate inspiratory flow rates to patients with heightened respiratory drive commonly results in dyspnea that may present as agitation

Clinical Findings

The history should focus on onset and timing of symptoms, the patient s position at onset of symptoms, the relationship of symptoms to activity, and any factors that may improve or exacerbate symptoms Complete allergic, occupational, and smoking histories are essential Exertional dyspnea should be quantified, but the absolute level of exertion that precipitates dyspnea is less important than acute changes in the threshold level of activity The clinician can assess dyspnea and response to treatment with a numeric rating scale by asking the patient, On a scale of zero to ten, with zero being no shortness of

breath and ten being the worst shortness of breath you can imagine, how short of breath are you Acute dyspnea has a short list of causes, most of which are readily identified: asthma, pulmonary infection, pulmonary edema, pneumothorax, pulmonary embolus, metabolic acidosis, or acute respiratory distress syndrome (ARDS) Panic attacks may present as a respiratory complaint Orthopnea (dyspnea on recumbency) and nocturnal dyspnea suggest asthma, gastroesophageal reflux disease, left ventricular dysfunction, or obstructive sleep apnea Rapid onset of severe dyspnea when supine suggests phrenic nerve impairment leading to diaphragmatic weakness or paralysis Platypnea (dyspnea that worsens in the upright position) is a rare complaint associated with arteriovenous malformations at the lung bases or with hepatopulmonary syndrome, resulting in increased shunting and hypoxemia in the upright position (orthodeoxia) Chronic dyspnea is typically progressive Symptoms often first appear during exertion; patients learn to limit their activity to accommodate their diminished pulmonary reserve until dyspnea occurs with minimal activity or at rest Episodic dyspnea suggests congestive heart failure, asthma, acute or chronic bronchitis, or recurrent pulmonary emboli Constant dyspnea is most commonly due to COPD but may indicate interstitial lung disease (eg, pulmonary fibrosis), pulmonary vascular disease, or fixed airflow obstruction from severe asthma Evaluation should include a complete blood count, renal function tests, chest radiograph, spirometry, and noninvasive oximetry Patients over 40 years of age or with a family history of early coronary disease should have an electrocardiogram Arterial blood gases, measurement of lung volumes, ventila tion-perfusion ( V/ Q) scanning, echocardiography, and cardiopulmonary exercise testing are reserved for cases that elude diagnosis on initial evaluation